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Health

Only 26% of adults survive acute myloid leukemia. Cincinnati Children's may have discovered a way to stop its progression

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Cincinnati Children's
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Microscopic slide: Compared to wild type control mice (left), mice receiving transplanted bone marrow cells that lacked functional versions of the genes TRAF6 and Tet2 developed neutrophilia, lymphopenia, and mild anemia—all signs of increased leukemia risk, according to research led by experts at Cincinnati Children’s.

The gene TRAF6 can block progression from pre-leukemia to full-blown disease, say researchers. But research is still in the early stages and potential therapies and clinical trials may be years away.

What makes acute myeloid leukemia (AML) so concerning is symptoms for the blood and bone marrow cancer can appear suddenly, and the five-year survival rate for adults is a disappointing 26%. It’s 70% for children.

For two years, Cincinnati Children’s Hospital cancer researcher Daniel Starczynowski, Ph.d., has been looking for ways to improve the odds. Now he and other scientists from NYU and Japan have apparently discovered a gene that can block the progression from pre-leukemia to full-blown disease.

The study, in collaboration with Iannis Aifantis, Ph.d., and his team at NYU, sheds new light on chain reactions which cause AML. The research is published Jan. 18, 2022 in Cell Stem Cell

What is this gene and how can it help?

The gene TRAF6 is a complex and key player when it comes to cancer, researchers say. Too much activity involving TRAF6 can lead to certain types of cancer risk. Not enough activity increases the risk of certain subtypes of AML. Restoring balance to the body appears to improve survival once the disease appears, at least in mice.

“The role of TRAF6 has been investigated for its role in immune cell biology," Starczynowski says. "However, more recently it has come to the forefront as a complex and key player in cancer. Some research indicates that it acts as a tumor suppressor, while others have reported that it can cause cancer."

He adds, “Our findings confirm that TRAF6 can, in fact, have opposite effects depending on the context of its environment. But we also found that its activity can be regulated through activation of certain toll-like receptors – evolutionarily conserved pathogen detectors in our immune systems that have been hijacked by the AML cell."

For patients, this means research is still in the early stages and potential therapies and clinical trials may be years away.

Starczynowski is now launching a series of experiments to understand why TRAF6 can function as both a tumor suppressor and a gene that is mutated. This could help in the emerging field of inflammation-targeted therapies.